Affinage

NEK8

Serine/threonine-protein kinase Nek8 · UniProt Q86SG6

Length
692 aa
Mass
74.8 kDa
Annotated
2026-06-10
32 papers in source corpus 23 papers cited in narrative 23 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

NEK8 is a NIMA-related serine/threonine kinase that couples a proximal ciliary signaling module to nuclear genome-protection and growth-control pathways, and is a cause of nephronophthisis and cystic kidney disease (PMID:23973373, PMID:37598857). The protein combines an N-terminal catalytic domain, a central RCC1-homology domain, and a C-terminal coiled-coil region, exhibits cell-cycle-independent autophosphorylation and oligomerization, and phosphorylates substrates including BICD2 (PMID:11864968). NEK8 localizes to centrosomes and to the proximal 'inversin compartment' of primary cilia, where INVS/inversin anchors NEK8 and NPHP3 and acts genetically upstream, ANKS6 bridges NEK8 to the INVS-NPHP3 module and activates the kinase by binding its catalytic domain, and disease-associated RCC1-domain mutations disrupt this targeting (PMID:18199800, PMID:20169535, PMID:23793029, PMID:25599650). Centrosome recruitment is driven by the RCC1 domain but depends on autophosphorylation-induced conformational change, and ciliogenesis triggers both kinase activation and proteasomal degradation (PMID:22106379). Within this compartment NEK8 binds polycystin-2 and is required for PC2-dependent mechanosensory responses to fluid shear stress, nodal ciliary signaling, and left-right patterning (PMID:18235101, PMID:23274954). In the nucleus NEK8 limits replication stress by suppressing cyclin A–CDK activity downstream of ATR, and promotes RAD51 loading and protection of stalled replication forks (PMID:23973373, PMID:27892797). NEK8 also controls Hippo signaling by directly binding the effectors TAZ and YAP to govern their nuclear delivery and target-gene output, and in cancer contexts phosphorylates c-MYC at Ser405, ASNS at Ser349, and LDHA to drive protein stabilization, mTORC1 activation, and metabolic reprogramming (PMID:23026745, PMID:26967905, PMID:37596667, PMID:39762761, PMID:41904143).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2002 Medium

    Established NEK8 as an active autophosphorylating kinase with a defined three-domain architecture and a first candidate substrate, framing it as a catalytic enzyme rather than a passive scaffold.

    Evidence Biochemical purification, in vitro kinase assay, and co-IP from rabbit lung

    PMID:11864968

    Open questions at the time
    • BICD2 phosphorylation site and its physiological consequence not defined
    • no cellular pathway context established
    • beta-casein is a generic substrate, not a physiological one
  2. 2008 Medium

    Localized NEK8 to the proximal cilium and centrosome and showed disease-associated RCC1-domain mutations selectively disrupt targeting, linking the kinase to ciliary biology and human nephropathy.

    Evidence GFP-tagged construct localization in kidney epithelial cells with multiple disease mutants

    PMID:18199800

    Open questions at the time
    • overexpression-based, no endogenous validation
    • mechanism of how RCC1 mutations block targeting unresolved
  3. 2008 Medium

    Connected NEK8 to polycystin signaling by demonstrating a selective interaction with polycystin-2 and showing the jck mutation alters PC2 phosphorylation and ciliary trafficking.

    Evidence Reciprocal co-IP, RT-PCR, and immunofluorescence in jck mouse kidneys

    PMID:18235101

    Open questions at the time
    • whether NEK8 directly phosphorylates PC2 not shown
    • single lab
  4. 2010 Medium

    Defined the hierarchy of the inversin compartment by showing INV anchors NEK8 and NPHP3, placing NEK8 downstream within a ciliary scaffold.

    Evidence Immunofluorescence and knockdown epistasis in inv mutant mouse cells

    PMID:20169535

    Open questions at the time
    • direct INV-NEK8 binding interface not mapped
    • functional consequence of mislocalization not assayed
  5. 2011 High

    Resolved the activation logic of NEK8: the RCC1 domain provides targeting but requires autophosphorylation-driven conformational activation, and ciliogenesis triggers degradation, establishing a regulated activation-turnover cycle.

    Evidence In vitro kinase assays, domain-deletion constructs, and proteasome inhibition with localization in mammalian cells

    PMID:22106379

    Open questions at the time
    • E3 ligase mediating degradation not identified
    • autophosphorylation sites not fully mapped
  6. 2012 High

    Demonstrated NEK8 is required in vivo for left-right patterning and PC2-dependent mechanosensing, separating its signaling role from ciliogenesis itself.

    Evidence Nek8-null mice, co-IP, fluid shear-stress assay, and zebrafish morpholino knockdown

    PMID:23274954

    Open questions at the time
    • how NEK8 enables PC2 mechanotransduction mechanistically unresolved
    • kinase-substrate relationship with PC2 not established
  7. 2012 Medium

    Confirmed by rescue epistasis that NEK8 acts genetically downstream of INV, and identified TAZ as a direct binding partner whose nuclear delivery NEK8 promotes, opening a Hippo-pathway dimension to NEK8 function.

    Evidence Zebrafish morpholino rescue epistasis; co-IP, fractionation, and proliferation assays for TAZ

    PMID:22687244 PMID:23026745

    Open questions at the time
    • whether NEK8 phosphorylates TAZ unresolved
    • competition with 14-3-3 inferred indirectly
  8. 2013 High

    Identified ANKS6 as the bridge connecting NEK8 to the INVS-NPHP3 module and (in 2015) as a direct activator binding the NEK8 kinase domain, unifying the genetics of overlapping ciliopathies.

    Evidence Complex purification, animal-model knockdown, hydroxylation assay; later mouse point-mutant alleles with in vitro kinase activation assay

    PMID:23793029 PMID:25599650

    Open questions at the time
    • structural basis of ANKS6-mediated activation not solved
    • physiological substrates downstream of activated NEK8 in the IC not defined
  9. 2013 High

    Established a nuclear genome-maintenance role: NEK8 suppresses cyclin A–CDK activity downstream of ATR to prevent replication stress, with a nephronophthisis allele specifically disrupting this function.

    Evidence Knockdown, DNA fiber assay, CDK activity assay, gammaH2AX foci, and mutant mouse kidney immunostaining

    PMID:23973373

    Open questions at the time
    • direct CDK-regulatory substrate of NEK8 not identified
    • how a ciliary kinase accesses the replication compartment unresolved
  10. 2013 Medium

    Linked NEK8 loss to dysregulated polycystin expression, c-MYC upregulation, and TAZ activation, tying ciliopathy phenotypes to transcriptional and growth-control outputs.

    Evidence Patient-derived fibroblasts, co-IP, western blot, RT-PCR

    PMID:23418306

    Open questions at the time
    • causal ordering between these outputs not established
    • single patient-derived model
  11. 2016 Medium

    Extended the replication-protection role to homologous recombination, showing NEK8 is required for RAD51 loading and protection of stalled forks, and refined Hippo control by showing NEK8 mutations imbalance YAP with rescue by YAP inhibition.

    Evidence Nek8-knockout MEFs with DNA fiber and RAD51 loading assays; patient fibroblasts, 3D spheroids, zebrafish, and Verteporfin rescue

    PMID:26967905 PMID:27892797

    Open questions at the time
    • whether NEK8 phosphorylates RAD51 or a loading factor unknown
    • direct YAP versus TAZ specificity not dissected
  12. 2023 High

    Tied human autosomal dominant PKD variants to reduced kinase activity, impaired ciliary PC2 localization, and elevated DNA damage, integrating the ciliary and genome-maintenance functions into disease mechanism, and identified c-MYC Ser405 as a stabilizing phosphosite in cancer.

    Evidence In vitro kinase assays, knockout-cell rescue with variants, ciliary PC2 and gammaH2AX imaging in patient tubuloids; phospho-specific and ubiquitination assays for c-MYC

    PMID:37596667 PMID:37598857

    Open questions at the time
    • how reduced kinase activity simultaneously affects cilia and replication not mechanistically linked
    • c-MYC ubiquitination machinery engaged by NEK8 unidentified
  13. 2025 Medium

    Expanded the NEK8 substrate and regulator network in cancer: NEK8 phosphorylates and stabilizes ASNS to activate mTORC1, drives WNT/beta-catenin signaling, and is itself stabilized by the deubiquitinase USP51.

    Evidence Co-IP, in vitro kinase and ubiquitination assays, mutagenesis, metabolic profiling, and rescue experiments in gastric and colorectal cancer cells

    PMID:39762761 PMID:41475333

    Open questions at the time
    • whether WNT activation is direct or downstream of metabolic effects unclear
    • single lab per substrate
  14. 2025 Medium

    Showed NEK8 overexpression phenocopies the HR/fork-protection defect of NEK8 loss and sensitizes cells to PARP inhibition, indicating dosage-sensitive control of genome maintenance.

    Evidence Overexpression with RAD51 foci, DNA fiber, and Olaparib sensitivity assays

    PMID:41101173

    Open questions at the time
    • mechanism reconciling loss and gain producing similar defects unresolved
    • single lab
  15. 2026 Medium

    Connected NEK8 kinase activity to tumor immune evasion by phosphorylating LDHA to drive lactate production, with pharmacological inhibition restoring CD8+ T cell function after radiotherapy.

    Evidence In vitro kinase assay, histone modification analysis, T cell assays, CX6258 inhibition, and in vivo tumor model

    PMID:41904143

    Open questions at the time
    • LDHA phosphosite and its enzymatic effect not fully defined
    • single lab

Open questions

Synthesis pass · forward-looking unresolved questions
  • How a single kinase coordinates its ciliary inversin-compartment signaling with nuclear replication-stress control, and what physiological substrates link these compartments, remains the central open question.
  • no unifying substrate connecting ciliary and nuclear roles identified
  • structural basis of RCC1/kinase domain coordination unsolved
  • spatial regulation directing NEK8 between cilium, centrosome, and nucleus unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 6 GO:0016740 transferase activity 3 GO:0098772 molecular function regulator activity 2
Localization
GO:0005929 cilium 4 GO:0005634 nucleus 2 GO:0005815 microtubule organizing center 2
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-73894 DNA Repair 3 R-HSA-1266738 Developmental Biology 2
Partners
ANKS6ASNSINVSNPHP3PKD2TAZUSP51YAP1
Complex memberships
inversin compartment (INVS-ANKS6-NPHP3-NEK8 module)

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 NEK8 was isolated as a beta-casein kinase activity and shown to have an N-terminal catalytic domain, a central RCC1-homology domain, and a C-terminal coiled-coil domain. It prefers beta-casein as substrate, is capable of autophosphorylation and oligomerization, and its kinase activity is not cell-cycle regulated. BICD2 (Bicaudal D2) was identified as a candidate substrate: NEK8 phosphorylates BICD2 in vitro, and the endogenous proteins co-immunoprecipitate in vivo. Biochemical purification from rabbit lung, in vitro kinase assay, co-immunoprecipitation, subcellular localization The Journal of biological chemistry Medium 11864968
2004 Overexpression of a kinase-domain-mutant NEK8 in U2-OS cells led to a decrease in actin protein and a small increase in CDK1/cyclin B1 levels, suggesting a functional link to cytoskeletal regulation and G2/M progression. Overexpression of kinase-dead mutant in mammalian cells, western blot Gene Low 15019993
2008 NEK8 localizes to the proximal portion of primary cilia and centrosomes in kidney epithelial cells; disease-associated RCC1-domain mutations (L330F, H425Y, A497P) disrupt ciliary and centrosomal localization without affecting ciliogenesis, mitosis, or centriole number. GFP-tagged construct overexpression in IMCD-3 cells, fluorescence microscopy Journal of the American Society of Nephrology : JASN Medium 18199800
2008 NEK8 co-immunoprecipitates with polycystin-2 (PC2) but not polycystin-1 (PC1) in kidney tissue. The jck mutation does not abolish the NEK8-PC2 interaction but leads to abnormal phosphorylation of PC2, elevated PC1 and PC2 expression/mRNA, and ciliary accumulation of PC1 and PC2. Co-immunoprecipitation, western blot, real-time RT-PCR, immunofluorescence in jck mouse kidneys Journal of the American Society of Nephrology : JASN Medium 18235101
2008 Mutations in the kinase and C-terminal RCC1 domains of NEK8 adversely affect ciliary targeting but do not affect ciliogenesis or ciliary length, indicating that kinase activity and the RCC1 domain are both required for proper ciliary localization. GFP-tagged constructs transiently expressed in vitro, fluorescence microscopy Pediatric nephrology (Berlin, Germany) Low 18189147
2010 Inv/NPHP2 acts as a molecular anchor for Nphp3 and Nek8 in the proximal ciliary 'Inv compartment'; Inv is essential for compartmental localization of both Nphp3 and Nek8, whereas the localization of Inv itself does not require Nphp3 or Nek8, placing Nek8 downstream of Inv in this ciliary scaffold. Immunofluorescence localization in inv mutant mouse cells, genetic epistasis by knockdown Cytoskeleton (Hoboken, N.J.) Medium 20169535
2011 NEK8 kinase activity is required for its own correct localization: the kinase domain alone is active but does not localize correctly, while the RCC1 domain localizes correctly and can be phosphorylated by NEK8. Centrosome recruitment is mediated by the RCC1 domain but requires autophosphorylation-induced conformational change. Induction of ciliogenesis upon cell cycle exit is accompanied by both activation and proteasomal degradation of Nek8, with activation dependent on phosphorylation within the catalytic domain. Nek8 kinase assays (in vitro), domain-deletion constructs, proteasome inhibitor treatment, fluorescence localization in mammalian cells Human molecular genetics High 22106379
2012 NEK8-null mice die at birth with randomized left-right asymmetry and cardiac anomalies; Nek8 is required for nodal ciliary signaling (left-sided marker genes are misexpressed without ciliogenesis defect). NEK8 and polycystin-2 (PC2) proteins interact by co-IP; Nek8-null embryos express PC2 normally and PC2 localizes properly to cilia, but NEK8-depleted IMCD cells exhibit a defective response to fluid shear stress similar to cells lacking PC2. Nek8-null mouse generation, co-immunoprecipitation, fluid shear-stress assay, zebrafish morpholino knockdown Journal of the American Society of Nephrology : JASN High 23274954
2012 Nek8 acts genetically downstream of Inv in zebrafish: nek8 mRNA rescues inv morphant phenotypes (pronephric cysts and cardiac looping defects), but inv mRNA cannot rescue nek8 morphant phenotypes. Simultaneous knockdown of nek8 and inv synergistically increases defect incidence. Zebrafish morpholino knockdown, mRNA rescue epistasis experiments FEBS letters Medium 22687244
2012 NPHP9/NEK8 directly interacts with TAZ (a Hippo pathway effector) and induces nuclear translocation of the TAZ/NPHP9 complex. Binding of NPHP9 to TAZ is enhanced in a TAZ mutant unable to bind 14-3-3, suggesting competitive binding: 14-3-3 favors cytoplasmic retention of TAZ whereas NPHP9 mediates nuclear delivery. Downregulation of NPHP9 inhibits TAZ-dependent cell proliferation. Co-immunoprecipitation, nuclear/cytoplasmic fractionation, fluorescence microscopy, siRNA knockdown with proliferation assay Human molecular genetics Medium 23026745
2013 ANKS6 connects NEK8 to the INVS-NPHP3 module at the proximal cilium. ANKS6 is hydroxylated by HIF1AN (as is INVS), which alters the composition of the ANKS6-INVS-NPHP3 complex. Network analysis places ANKS6 at the center of this NPHP module, explaining overlapping disease manifestations from mutations in ANKS6, NEK8, INVS, or NPHP3. Co-immunoprecipitation/complex purification, zebrafish and Xenopus knockdown, hydroxylation assay (HIF1AN), network analysis Nature genetics High 23793029
2013 NEK8 is a key effector of ATR-mediated replication stress response: cells lacking NEK8 form spontaneous DNA double-strand breaks, show reduced replication fork rates, unscheduled origin firing, and increased fork collapse. NEK8 suppresses DSB formation by limiting cyclin A-associated CDK activity. A nephronophthisis-associated mutation in NEK8 specifically disrupts its genome maintenance function, and kidneys of NEK8-mutant mice accumulate DNA damage. siRNA/shRNA knockdown, DNA fiber assay, γH2AX foci, replication origin firing assay, CDK activity assay, mouse kidney immunostaining Molecular cell High 23973373
2013 NEK8 loss-of-function mutations reduce PKD1 and PKD2 expression, upregulate c-MYC, and activate the Hippo effector TAZ. NEK8 and NPHP3 interact by co-immunoprecipitation and together activate TAZ. Patient-derived fibroblasts (loss-of-function due to nonsense-mediated decay), co-immunoprecipitation, western blot, RT-PCR Human molecular genetics Medium 23418306
2015 ANKS6 is both a target and an activator of NEK8: ANKS6 requires NEK8 for localization to the ciliary inversin compartment (IC), and ANKS6 activates NEK8 by binding to its kinase domain. The Nek8(Roc) mutation inactivates NEK8 kinase function while preserving ANKS6 localization to the IC. The Anks6(Strkr) mutation decreases ANKS6-NEK8 interaction, precluding NEK8 activation. Mouse genetic models (Anks6^Streaker and Nek8^Roc point mutations), co-immunoprecipitation, in vitro kinase activity assay, immunofluorescence localization Nature communications High 25599650
2016 NEK8 regulates the Hippo pathway effector YAP: NEK8 missense and loss-of-function mutations differentially affect YAP levels and its target gene expression in patient fibroblasts and renal cells. YAP imbalance was observed in Nek8-invalidated 3D spheroids and in cystic kidneys of jck mice. Inhibition of YAP with Verteporfin partially rescued 3D spheroid defects in Nek8-null cells and abnormalities in NEK8-overexpressing zebrafish embryos. Patient fibroblasts, mIMCD3 cells, 3D culture, zebrafish co-injection, Verteporfin pharmacological rescue, western blot for YAP target genes PLoS genetics Medium 26967905
2016 NEK8 is required for efficient DNA damage-induced RAD51 foci formation and replication fork protection. NEK8 knockout cells show decreased RAD51 loading onto chromatin and nascent DNA tract degradation following replication stalling (hydroxyurea). Loss of NEK8 causes increased chromosome breaks after hydroxyurea treatment. siRNA screen, Nek8-knockout MEFs, DNA fiber assay, RAD51 chromatin loading assay, immunofluorescence foci Cell cycle (Georgetown, Tex.) Medium 27892797
2022 NEK8 interacts with TAZ in adipocytes (co-immunoprecipitation) and suppresses TAZ expression, promoting adipocyte differentiation and lipid accumulation. Lentiviral NEK8 inhibition ameliorates high-fat diet-induced insulin resistance in a mouse model. Co-immunoprecipitation, confocal immunofluorescence, shRNA knockdown, western blot, in vivo HFD mouse model Oxidative medicine and cellular longevity Low 36506932
2023 NEK8 phosphorylates c-MYC at serine 405 in colorectal cancer cells, which enhances c-MYC protein stability via polyubiquitination. In vitro kinase assay, phospho-specific antibody, ubiquitination assay, site-directed mutagenesis (S405A), western blot Cell communication and signaling : CCS Medium 37596667
2023 NEK8 kinase-domain missense variants (e.g. p.Arg45Trp, p.Lys157Gln) associated with autosomal dominant PKD show reduced kinase activity in vitro, decrease polycystin-2 (but not ANKS6) localization in cilia, and increase DNA damage signaling (γH2AX) in patient-derived tubuloids and IMCD3 cells. In vitro kinase assay, Nek8-knockout IMCD3 cell rescue with variant constructs, immunofluorescence for ciliary polycystin-2, γH2AX foci in patient tubuloids Kidney international High 37598857
2025 USP51, a deubiquitinase, directly interacts with NEK8 (co-immunoprecipitation, co-immunofluorescence) and lowers the ubiquitination level of NEK8 protein, thereby stabilizing it. NEK8 promotes colorectal cancer progression partly via activation of the WNT/β-catenin pathway, as NEK8 knockdown decreases β-catenin protein levels. Co-immunoprecipitation, co-immunofluorescence, ubiquitination assay, functional rescue experiments, western blot for β-catenin Pathology, research and practice Medium 41475333
2025 NEK8 directly interacts with asparagine synthetase (ASNS) and phosphorylates it at serine 349, inhibiting ASNS ubiquitination and degradation. This stabilization of ASNS promotes asparagine synthesis and activates the mTORC1 pathway in gastric cancer cells. Co-immunoprecipitation, in vitro kinase assay, ubiquitination assay, site-directed mutagenesis (ASNS-S349A), metabolic profiling, mTORC1 pathway readouts Molecular medicine (Cambridge, Mass.) Medium 39762761
2025 NEK8 overexpression inhibits RAD51 focus formation, causes a defect in homologous recombination, and leads to degradation of stalled replication forks. NEK8-overexpressing cells are sensitized to the PARP inhibitor Olaparib. NEK8 overexpression in mammalian cells, RAD51 immunofluorescence foci, DNA fiber assay, Olaparib sensitivity assay DNA repair Medium 41101173
2026 NEK8 phosphorylates lactate dehydrogenase A (LDHA), driving lactate overproduction in colorectal cancer cells. Elevated lactate promotes histone modifications silencing antigen presentation machinery and impairs CD8+ T cell function. Pharmacological NEK8 inhibition with CX6258 restores CD8+ T cell infiltration and enhances tumor control after radiotherapy. In vitro kinase assay (NEK8 phosphorylating LDHA), histone modification analysis, CD8+ T cell functional assays, pharmacological inhibition (CX6258), in vivo tumor model Nature communications Medium 41904143

Source papers

Stage 0 corpus · 32 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 ANKS6 is a central component of a nephronophthisis module linking NEK8 to INVS and NPHP3. Nature genetics 170 23793029
2008 NEK8 mutations affect ciliary and centrosomal localization and may cause nephronophthisis. Journal of the American Society of Nephrology : JASN 168 18199800
2013 NEK8 links the ATR-regulated replication stress response and S phase CDK activity to renal ciliopathies. Molecular cell 118 23973373
2008 Nek8 regulates the expression and localization of polycystin-1 and polycystin-2. Journal of the American Society of Nephrology : JASN 95 18235101
2004 Nek8, a NIMA family kinase member, is overexpressed in primary human breast tumors. Gene 87 15019993
2013 Mutations in NEK8 link multiple organ dysplasia with altered Hippo signalling and increased c-MYC expression. Human molecular genetics 83 23418306
2010 Inv acts as a molecular anchor for Nphp3 and Nek8 in the proximal segment of primary cilia. Cytoskeleton (Hoboken, N.J.) 82 20169535
2016 Novel NEK8 Mutations Cause Severe Syndromic Renal Cystic Dysplasia through YAP Dysregulation. PLoS genetics 76 26967905
2012 The ciliopathy disease protein NPHP9 promotes nuclear delivery and activation of the oncogenic transcriptional regulator TAZ. Human molecular genetics 67 23026745
2011 The Nek8 protein kinase, mutated in the human cystic kidney disease nephronophthisis, is both activated and degraded during ciliogenesis. Human molecular genetics 60 22106379
2012 A novel mutation causing nephronophthisis in the Lewis polycystic kidney rat localises to a conserved RCC1 domain in Nek8. BMC genomics 57 22899815
2013 Loss of the ciliary kinase Nek8 causes left-right asymmetry defects. Journal of the American Society of Nephrology : JASN 52 23274954
2002 Purification, cloning, and characterization of Nek8, a novel NIMA-related kinase, and its candidate substrate Bicd2. The Journal of biological chemistry 51 11864968
2015 ANKS6 is the critical activator of NEK8 kinase in embryonic situs determination and organ patterning. Nature communications 47 25599650
2005 Nek8 mutation causes overexpression of galectin-1, sorcin, and vimentin and accumulation of the major urinary protein in renal cysts of jck mice. Molecular & cellular proteomics : MCP 43 15872312
2007 Pkd1 and Nek8 mutations affect cell-cell adhesion and cilia in cysts formed in kidney organ cultures. American journal of physiology. Renal physiology 42 17928412
2023 Certain heterozygous variants in the kinase domain of the serine/threonine kinase NEK8 can cause an autosomal dominant form of polycystic kidney disease. Kidney international 36 37598857
2008 Defects in ciliary localization of Nek8 is associated with cystogenesis. Pediatric nephrology (Berlin, Germany) 30 18189147
2016 NEK8 regulates DNA damage-induced RAD51 foci formation and replication fork protection. Cell cycle (Georgetown, Tex.) 23 27892797
2013 Nek8 couples renal ciliopathies to DNA damage and checkpoint control. Molecular cell 22 23973371
2012 The ciliary protein Nek8/Nphp9 acts downstream of Inv/Nphp2 during pronephros morphogenesis and left-right establishment in zebrafish. FEBS letters 19 22687244
2015 Compound heterozygous mutations in NEK8 in siblings with end-stage renal disease with hepatic and cardiac anomalies. American journal of medical genetics. Part A 18 26697755
2023 NEK8 regulates colorectal cancer progression via phosphorylating MYC. Cell communication and signaling : CCS 12 37596667
2025 NEK8 promotes the progression of gastric cancer by reprogramming asparagine metabolism. Molecular medicine (Cambridge, Mass.) 7 39762761
2022 NEK8-Associated Nephropathies: Do Autosomal Dominant Forms Exist? Nephron 6 36215968
2025 NEK8, a NIMA-family protein kinase at the core of the ciliary INV complex. Cell communication and signaling : CCS 4 40189576
2022 Never-in-Mitosis A-Related Kinase 8 (NEK8) Regulates Adipogenesis, Glucose Homeostasis, and Obesity. Oxidative medicine and cellular longevity 4 36506932
2026 Multi-omics profiling of sodium-overload (NECSO) programs identifies NEK8 as a central driver of colorectal cancer progression through single-cell and spatial transcriptomics. Frontiers in immunology 0 41743703
2026 NEK8 kinase-mediated lactate increase impairs antitumor immunity decreasing radiotherapy sensitivity in colorectal cancer. Nature communications 0 41904143
2025 Overexpression of the NEK8 kinase inhibits homologous recombination. bioRxiv : the preprint server for biology 0 39975112
2025 Overexpression of the NEK8 kinase inhibits homologous recombination. DNA repair 0 41101173
2025 NEK8 stabilization via USP51-mediated deubiquitination promotes colorectal cancer progression. Pathology, research and practice 0 41475333

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